The prevalence of chronic liver disease has escalated rapidly worldwide due to the rising number of people inflicted with alcoholism, chronic hepatitis B infection, chronic hepatitis C infection, diabetes, and obesity. During fibrosis and pre-cirrhosis, hepatic stellate cells (HSCs) are activated and deposit fibrous collagen into the space of Disse. As a result, the normal liver architecture is destroyed and normal liver cells, called hepatocytes, can no longer exchange nutrients and wastes with the blood plasma. This ultimately results in cirrhosis, the formation of regenerative nodules of hepatocytes surrounded by fibrous scar tissue. During cirrhosis, the risk of developing hepatocellular carcinoma (HCC) is dramatically elevated as HCC develops in a step-wise progression from regenerative nodules to dysplastic nodules to well-differentiated tumors. Treatment options for HCC are currently ineffective, and as such, HCC is one of the few cancers where the incidence and mortality rates are equal. Therefore, early intervention to reduce fibrosis and pre-cirrhosis and the risk of developing macronodular cirrhosis and HCC would be desirable.